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7/28/2019 Acute renal failure J REignier SarajevoSept2010.pdf
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AcuteRenal
Failure
Dr Jean ReignierPrsident de la Socit de Ranimation de Langue Franaise
Service de Ranimation. La Roche-sur-Yon.
www.srlf.org
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Definition of ARF AKI
Jean Reignier, Sarajevo 2010
No universal objective definition.
an abrupt and sustained decrease in renal function resulting in
retention of nitrogenous (urea and creatinine) and non nitrogenous
waste products .
An abrupt (within 48 hours) reduction in kidney function currently
defined as an absolute increase in serum creatinine of more than or
equal to 0.3 mg/dl ( 26.4 mol/l), a percentage increase in serum
creatinine of more than or equal to 50% (1.5-fold from baseline), or a
reduction in urine output (documented oliguria of less than 0.5 ml/kg
per hour for more than six hours)
Crit Care 2007
ARF Acute Kidney Injury ( Insufficiency )
RIFLE and AKIN definition and classification schemes
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Jean Reignier, Sarajevo 2010
Definition of ARF AKI
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Jean Reignier, Sarajevo 2010
Definition of ARF AKI
1. Diagnosis of AKI is based on changes over the course of 48 hours.
2. The therapy for AKI (RRT) was not include as a distinct stage because this constitutes an outcome
of AKI.
3. The new staging system maps to the RIFLE stages as follows:
3a. RIFLE 'Risk' category should have the same criteria as for the diagnosis of stage 1 AKI.
3b. Those who are classified as having 'Injury' and 'Failure' cat- egories map to stages 2 and 3 of
AKI.
3c. The 'Loss' and 'End-stage kidney disease' categories were removed from the staging system and
remain outcomes.3d. Given the variability inherent in commencing RRT and due to variability in resources in different
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Jean Reignier, Sarajevo 2010
The continuum of the renal (kidney)
injury
Stage 1:
Risk
Stage 2:
InjuryStage 3:
Failure Loss ESRD
The stages before failure are of high clinical
interest for prevention and therapeutic
interventions.
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Incidence of AKI
Severe ARF requiring dialysis
Overall population in UK: 22 cases per million adults per year (BMJ1993)
In hospital: 131 cases per million adults per year (QJM2002)
In ICU:
Incidence of AKI varies (1-25%) with definition of AKI and study
populations.
In many cases accompagnied with multiorgan failure +++
AKI requiring Renal Replacement Therapy : 5-6% of ICU patients
ARF and sepsis:
Moderate sepsis: 19%
Severe sepsis: 23%
Sepsic shock with positive blood culture: 51% (SchrierNEJM2004)
Jean Reignier, Sarajevo 2010
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To function properly kidneys
require :
Normal renal blood flow
Functioning glomeruli and tubules
Clear urinary outflow tract
Jean Reignier, Sarajevo 2010
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Renal Blood Flow = blood
perfusing the kidney
(approx. 20% of cardiac
blood flow = 1200ml/min)
Renal Plasma Flow =
plasma perfusing the
kidney (approx. 55-60% ofRBF = 650ml/min
Glomeruli Flow Rate =
amount of plasma filtered
every min by the glomeruli
(men: 125ml/min; women:
100ml/min)
Filtration Fraction =
GFR/RPF (18-22%)
Jean Reignier, Sarajevo 2010
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Afferent and efferent arterioles are the major sites of renalvascular resistance
Changes in resistance of afferent or efferent artioles affect RBF.
Jean Reignier, Sarajevo 2010
Afferent
arteriole
Efferent arterioles
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Jean Reignier, Sarajevo 2010
Abuelo NEJM2007
Renal autoregulation
breaks down when MAP
falls below 80mmHg
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+Causes of Acute Kidney Injury
The causes of AKI are classified as:
Prerenal = reduction in renal perfusion (30%)
Loss of intravascular volume
Obstruction of renal flow
Renal (Parenchymal) (65%):
Tubular disorders: Acute tubular ncrosis +++ (55%)
Vascular disorders (3%)
Glomerulonephritis (3%)
Interstitial nephritis (2%)
Post-renal (5%):
Extrarenal obstruction of the urinary tract
Intrarenal obstruction
Jean Reignier, Sarajevo 2010
Renal autoregulation
breaks down when MAP
falls below 80mmHg
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Hypovolemia
Hemorrage
Vomiting
Diarrhea
Burns
Jean Reignier, Sarajevo 2010
Prerenal AKI
Oedema states
Cardiac
failure
Cirrhosis
Nephrotic
syndrome
Hypotension
Cardiogenic
Initial Septic
schock
Anaphylaxis
Renal hypoperfusion
NSAID
ACEI/ARB
Renal artery
stenosis
Hepatorenal
syndrom
Decreased RBF
Reduced GFR
Prerenal AKI
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Renal hypoperfusion:
Increased Na and H20 reaborption
Oliguria
High U osm (>500), low Una (FeNa>1%)
Elevated BUN/S Cr Ratio
Jean Reignier, Sarajevo 2010
Prerenal AKI
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Sepsis 50%
Hemodynamic (non sepsis) 30%
Toxic 20%
NSAIDS
Radiocontrast media
Antiinfective drugs (Gentamicin, Amphotericin)
Jean Reignier, Sarajevo 2010
Acute tubular necrosis
Renal Tubular obstruction:
Oliguria
Low U osm (
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+ Effect of acute renal failure requiring renal replacement therapyon outcome in critically ill patients
Metnitz, Crit Care Med 2002
Patients AKI requiring Renal
Replacement Therapy:
62.8% mortality rate
AKI = independent riskfactor for death
Jean Reignier, Sarajevo 2010
17126 ICU patients : 839 with RTT vs 16287 without RTT
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+Outcome of ICU patients with AKI
However, cause of death unknown (cause and effect relation-ship or
AKI = marker of disease severity ?)
Numerous potential consequences of AKI:
Uremic intoxication
Induction of proinflammatory state by the injured kidney
Severe metabolic disorders
Fluid overload
Influence of the severity of underlying disease on outcome
Mortality and cause of AKI: ischemic (30%) / nephrotoxic (10%)
Predictors of mortality: RRT requirement, multiorgan failure (mechical
ventilation, hyperbilirubinemia, lactic acidosis)
Jean Reignier, Sarajevo 2010
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+AKI Consequences
Life-threatening:
Hyperkaliemia
Volume overload : Acute Pulmonary Edema
Metabolic Acidosis
Uremia:
Pericarditis
Encephalopathy
Platelet dysfunction
Jean Reignier, Sarajevo 2010
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+Markers of AKI
Sensitive and specific markers for kidney injury are not
currently available in clinical practice.Urinary output and serum creatinine are (remain) the
primary markers of AKI.
New markers are investigated.
Jean Reignier, Sarajevo 2010
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+Markers of AKI : Serum creatinine
Always available.
Consider factors affecting serum creatinine level when interpreting
results (body size, catabolic state, dilutional effects).
Refer to baseline level of the patient.
Observe changes in serum creatinine level (/6 hours)
Standard formulation for calculation of creatinine clearance do not
predict glomerular filtration rate in patients who are not in steady
state, and should not be used in ICU.
Jean Reignier, Sarajevo 2010
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+Markers of AKI : BUN
Affected by numerous factors (more than serum creatinine):
Protein loading
Catabolic state; severe sepsis GI bleeding
Corticosteroid therapy
Good correlation with uremic complications
Jean Reignier, Sarajevo 2010
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+AKI : Diagnostic approach
Acute or chronic Renal Failure ?
History and examination
Previous serum creatinine measurements
Ultrasonographic examination: Small kidney (except diabete)
Eliminate obstruction (post renal AKI): complete anuria,
Ultrasonographic examination
Is the patient hypovolemic?
History, HR, Cardiac ultrasonographic exam, weight, fluid balance
Increase in urea/creatinine ratio
low Una (FeNa>1%)
Fluid challenge
Eliminate major vascular occlusion? Jean Reignier, Sarajevo 2010
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+Prevention of AKI in ICU
Of particular importance regarding potential adverse effects of AKI and
worsening of outcome.
However, AKI involves multiple mechanisms in ICU patients
Prevention of AKI in ICU includes:
Adequate fluid resuscitation
Use of vasoactive drugs in patients with persistent shock after fluid
resuscitation Protection against nephrotoxic substances (antibiotics, radiocontrast
media)
Strategies adapted to specific diseases (liver disease, tumor lysis
syndrome, rhabdomyolysis).
Jean Reignier, Sarajevo 2010
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+Prevention of AKI in ICU
Essential to prevent or correct renal hypoperfusion (prerenal azotemia),
but not sufficient in many ICU patients with complex diseases involving
multiple mechanisms.
The optimal fluid resuscitation is unknown (no studies).
Use a Mean Arterial Pressure target:
At least 65 mmHg
>65 mmHg in the elderly or patients with a history ofhypertension
Use vasoactive drugs when fluid resuscitation is achieved.
Jean Reignier, Sarajevo 2010
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+Prevention of AKI in ICUUse of vasoactive drugs
Never use low-dose dopamine (does not protect from AKI although it
increases diuresis, could worsen renal perfusion and function in
patients with AKI. FriedrichAnnals of Intern Med2005)
Use vasopressor when MAP remains low (
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+Prevention of AKI in ICUProtection against nephrotoxic substances
Antibiotics:
Avoid nephrotoxic anti-infective (aminoglycosides) agents when
possible.
Avoid association between nephrotoxic anti-infective
(aminoglycosides) agents
Limit duration of therapy at the time really needed
Use appropriate dosage and dose interval (once a day for
aminoglycosides)
Ajust dosing according to renal clearance
Monitor antibiotic blood concentration
Radio-contrast media
Avoid the use of contrast medium when risks of AKI outweigh benefit
+++
Use low- or iso-osmolar contrast medium
Avoid other AKI risks factors (hypovolemia+++) Jean Reignier, Sarajevo 2010
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+Management of patients with AKI
Always keep in mind the potential reversibility of renal dysfunction in
many cases+++
Key points:
Restore hypovolemia with saline. Correct persistent hypotension with vasopressors (MAP > 65 mmHg).
Diuretics do not reduce mortality or morbidity and should not be
used before adequat fluid resuscitation.
Avoid or discontinue nephrotoxic substances:
Stop nonsteroidal anti-inflammatory drugs Avoid amino glycosides if alternative antibiotics are available
Avoid starches and dextrans
Limit the use of radiocontrast media
Jean Reignier, Sarajevo 2010
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+ Management of AKI : dialysis (Renal
Replacement Therapy)
Anticoagulation:
Is used to prevent clotting of the membrane and thus improve
efficacy of RRT and minimize blood loss in the circuit.
Unfractionned or low molecular weight heparin can be used.
Balance between risks of anticoagulant therapy (bleeding+++) and
risks of filter clotting (blood loss, decreased efficiency of RRT)
Patients treated with anticoagulant for a specific condition (atrialfibrillation ) do not require additional anticoagulation.
In patients with high risk of bleeding, anticoagulation should be
avoided and intermittent hemodialysis preferred.
Jean Reignier, Sarajevo 2010
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To improve hemodynamic tolerance:
Use dialysate with Na >145 mmol/l and with temperature between 35
and 37C. Avoid acetate buffered dialysate.
In unstable patients:
start intermittent hemodialysis without ultrafiltration
when hemofiltration is required, decrease ultration rate and
increase hemodialysis session duration.
Septic patients have poor tolerance of ultrafiltration.
Jean Reignier, Sarajevo 2010
Management of AKI : dialysis (Renal
Replacement Therapy)
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+Renal Replacement Therapy:
when?
RRT is an emergency in cases of:
Hyperkalemia
Pulmonary edema unresponsive to diuretics
Intractable acidosis
Aside from these life-threatening conditions, optimal time to
initiate RRT is unknown.
Doctors has to determine for each individualpatients the right moment to initiate RTT to avoid fluid
overload, clinically significant metabolic disorders and
bleeding.
Jean Reignier, Sarajevo 2010
R l R l t Th
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Jean Reignier, Sarajevo 2010
Renal Replacement Therapy:
intermittent or continuous?
BrochardAJRCCM2010
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+Renal Replacement Therapy:
intermittent or continuous?
Numerous studies showed that RRT mode had no impact on
mortality and renal recovery in a non-selected ICU population.
However, these two RTT modes exert significant modalities that
could be advantages or disadvantages for an individual patients. Schematically:
Patients with highly unstable shock may benefit from CRRT
Stable patients (the vast majority) require IHD
Patients with increased bleeding risk require IHD
Jean Reignier, Sarajevo 2010
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J R i i S j 2010
HVALA